The vagus nerve is the parasympathetic nervous system's pathway to the lungs. It affects airway muscle tone and mucus secretion. When the vagus nerve is stimulated, it releases acetylcholine, the cholinergic mediator. This mediator contracts the airway muscle and increases mucus production. Because this whole mechanism involves nerves, its effects are termed neurally mediated.
These cholinergic mediator effects can be stopped by a drug that blocks the action of acetylcholine. Atropine does just that. In fact, atropine inhalation was a standard asthma treatment until the 1930s, when the first crop of beta-stimulators (the general adrenaline imitators) rendered the side effects of atropine unacceptable. But though atropine was pushed off center stage, it never quite disappeared.
There is now new interest in anticholinergic bronchodilators spurred by two developments over the past 35 years. One is better understanding of the ways in which acetylcholine influences the diameter of healthy and diseased airways. Second has been development of effective atropine-like drugs thatunlike their parentare not absorbed into the general circulation. Local administration (by inhalation) of these atropine-derived drugs means much smaller doses are needed, and therefore side effects are much gentler.
The most extensively studied atropine derivative, ipratropium bromide, has been available since the early 1980s |
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